Association between endometriosis and obstetric complications: Insight from the National Inpatient Sample

Abu-Zaid, Ahmed; Gari, Abdulrahim; Tulbah, Maha; Alshahrani, Majed Saeed; Khadawardi, Khalid; Ahmed, Albagir Mahdi; Baradwan, Afnan; Bukhari, Ibtihal Abdulaziz; Alyousef, Abdullah; Alomar, Osama; Abuzaid, Mohammed; Baradwan, Saeed

doi:10.1016/j.ejogrb.2023.11.009

Cited by 5 publications

(1 citation statement)

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“…Women with poly cystic ovarian syndrome (PCOS) and hirsutism have higher than reference values for serum androgen and AR levels [51,52]. However, PCOS is significantly associated with higher risk of endometrial cancer but does not associate with higher risk of cervical cancers [53]; this supports a probable protectiveness of androgen and AR against cervical cancer development. However, further in depth research is warranted to reveal any such mechanistic connection.…”

Section: Discussionmentioning

confidence: 99%

Androgen receptor plays critical role in regulating cervical cancer cell migration

Bose,

Das,

Maity

et al. 2024

Preprint

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Cervical cancer (CC) is the second most common cancer among women in India and the fourth worldwide. While major genes and pathways have been studied, further research is needed to identify candidates for targeted therapy in metastatic disease. This study used a network biology approach to identify key genes in disease progression. Stage-specific cervical cancer protein-protein interaction networks (PPIN) were constructed by overlaying stage-specific, patient-derived transcriptomics data onto a human protein-protein interaction network (HPPIN). Graph-theory-based network analysis identified important interacting proteins (IIPs) with maximum connectivity, high centrality scores, and significant global and local network perturbation scores. Among the identified IIPs, the Androgen receptor (AR) emerged as one of the crucial yet understudied regulator in cervical cancer. Patient samples and in vitro experiments showed significant downregulation in cervical cancer. Ligand-dependent overexpression of AR reduced cancer cell migration while failed to induce apoptosis in CC cell lines. Downregulation of mesenchymal markers and restoration of epithelial markers suggested AR’s potential in reversing invasive properties of cervical cancer cells. AR overexpression upregulated its downstream target PTEN and restored GSK3β activity by interfering with AKT phosphorylation, probably leading to degradation of mesenchymal markers. Further studies showed AR reduced cell motility by hindering focal adhesion formation and Actin filament assembly. An increased G-Actin ratio suggested AR disrupted cytoskeletal dynamics through the RhoA/ROCK1/LIMK1/CFL1 pathway, impeding cervical cancer cell spread.

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Section: Discussionmentioning

confidence: 99%